Augusto Nogueira

Hospital de Santo António

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Rui Medeiros

Portuguese League Against Epilepsy

Joana Assis

Centro Hospitalar de Trás os Montes e Alto Douro

Raquel Catarino

Hospital Pedro Hispano

Deolinda Pereira

IPO Porto

Mónica Gomes

University of Minho

Helena Gervásio

University of Coimbra

P. Jacinto

Instituto Português de Oncologia de Coimbra Francisco Gentil

Nuno Bonito

Instituto Português de Oncologia de Coimbra Francisco Gentil

Joaquina Maurício

Instituto Português de Oncologia Francisco Gentil

Ana Coelho

Hospital de São João

Cooperative Institutions

Instituto Português de Oncologia Francisco Gentil

Universidade do Porto

IPO Porto

Instituto Português de Oncologia de Coimbra Francisco Gentil

University of Lisbon

i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto

Mayo Clinic

Mayo Clinic in Arizona

Centro Hospitalar do Porto

Centro Hospitalar de Lisboa Ocidental

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P-167 Cetuximab rechallenge in metastatic colorectal cancer patients

Annals of Oncology (2016)

Augusto Nogueira Joana Rodrigues P. Jacinto João Ribeiro Nuno Bonito

10.1093/annonc/mdw199.161

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Citations (4)

Non‐obstrutive dilatations of fetal urinary‐tract and bowel. A case report

International Journal of Gynecology & Obstetrics (2000)

Aderson Tadeu Berezowski Carolina Rocha Machado Felipe D’Almeida Costa Fadia Dib R. Cassoli

10.1016/s0020-7292(00)85286-8

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Common Genetic Polymorphisms in the ABCB1 Gene Are Associated with Risk of Major Depressive Disorder in Male Portuguese Individuals

Genetic Testing and Molecular Biomarkers (2013)

Marlene Santos Serafim Carvalho Luís Lima Augusto Nogueira Joana Assis

Major depressive disorder (MDD) is a highly prevalent disorder, which has been associated with an abnormal response of the hypothalamus-pituitary-adrenal (HPA) axis. Reports have argued that an abnormal HPA axis response can be due to an altered P-Glycoprotein (P-GP) function. This argument suggests that genetic polymorphisms in ABCB1 may have an effect on the HPA axis activity; however, it is still not clear if this influences the risk of MDD. Our study aims to evaluate the effect of ABCB1 C1236T, G2677TA and C3435T genetic polymorphisms on MDD risk in a subset of Portuguese patients. DNA samples from 80 MDD patients and 160 control subjects were genotyped using TaqMan SNP Genotyping assays. A significant protection for MDD males carrying the T allele was observed (C1236T: odds ratio (OR)=0.360, 95% confidence interval [CI]: [0.140-0.950], p=0.022; C3435T: OR=0.306, 95% CI: [0.096-0.980], p=0.042; and G2677TA: OR=0.300, 95% CI: [0.100-0.870], p=0.013). Male Portuguese individuals carrying the 1236T/2677T/3435T haplotype had nearly 70% less risk of developing MDD (OR=0.313, 95% CI: [0.118-0.832], p=0.016, FDR p=0.032). No significant differences were observed regarding the overall subjects. Our results suggest that genetic variability of the ABCB1 is associated with MDD development in male Portuguese patients. To the best of our knowledge, this is the first report in Caucasian samples to analyze the effect of these ABCB1 genetic polymorphisms on MDD risk.

SNP

10.1089/gtmb.2013.0197

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Citations (18)

The impact of GGH -401C>T polymorphism on cisplatin-based chemoradiotherapy response and survival in cervical cancer

Gene (2012)

Inês Hilário Silva Cristina Nogueira‐Silva Tiago Figueiredo Liliana Lombo I. Faustino

Chemoradiotherapy

SNP

Log-rank test

10.1016/j.gene.2012.10.038

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Citations (7)

DNA Damage Repair and Cancer: The Role of RAD51 Protein and Its Genetic Variants

InTech eBooks (2011)

Augusto Nogueira Raquel Catarino Rui Medeiros

Genomes are continually attacked by both endogenous and exogenous agents that damage DNA. DNA damage in the form of DNA breaks can lead to chromosome translocations, cell cycle arrest, and apoptosis. Homologous recombination is an essential biological process that ensures the accurate repair of DNA breaks and thereby contributes to genomic integrity (Kuzminov 1999; Paques and Haber 1999). DNA double-strand breaks (DSBs) are considered the principal lethal DNA damage resulting from ionizing radiation and cross-linking drugs. In addition, DSB can arise from endogenous processes, such as replication fork stalling during attempted replication over a single strand-break and topoisomerase poisons that are common therapies in the treatment of human cancers (Arnaudeau, Lundin et al. 2001). It is of great importance that cells recognise DSBs and act upon them rapidly and efficiently, because cell death or impaired cell function can occur if these are left unrepaired or are repaired inaccurately. In addition to DNA repair mechanisms, cell cycle checkpoint activation processes are initiated in response to DNA damage. More specifically, DNA damage signals to arrest cell cycle progression, giving the cell more time to repair what might otherwise be a fatal lesion (Henning and Sturzbecher 2003).

DNA Damage Repair

10.5772/23137

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Citations (4)

2031 Number of retrieved lymph nodes in gastric cancer patients and survival

European Journal of Cancer (2015)

Nadine Saraiva Ana Rita Garcia Augusto Nogueira Nuno Bonito P. Jacinto

10.1016/s0959-8049(16)30954-6

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Genetic variants as ovarian cancer first-line treatment hallmarks: A systematic review and meta-analysis

Cancer Treatment Reviews (2017)

Joana Assis Carina Pereira Augusto Nogueira Deolinda Pereira Rafael Carreira

ERCC1

10.1016/j.ctrv.2017.10.001

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Citations (17)

P-083 Prognostic determinants in gastric cancer survival - the importance of metastatic lymph node ratio

Annals of Oncology (2015)

Augusto Nogueira Ana Rita Garcia Nadine Saraiva João Ribeiro P. Jacinto

Chemoradiotherapy

10.1093/annonc/mdv233.83

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DNA repair and cytotoxic drugs: the potential role of RAD51 in clinical outcome of non-small-cell lung cancer patients

Pharmacogenomics (2013)

Augusto Nogueira Joana Assis Raquel Catarino Rui Medeiros

Many of the cytotoxic drugs used in the treatment of non-small-cell lung carcinoma patients can interfere with DNA activity and the definition of an individual DNA repair profile could be a key strategy to achieve better response to chemotherapeutic treatment. Although DNA repair mechanisms are important factors in the prevention of carcinogenesis, these molecular pathways are also involved in therapy response. RAD51 is a crucial element in DNA repair by homologous recombination and has been shown to interfere with the prognosis of patients treated with chemoradiotherapy. There is increasing evidence that genetic polymorphisms in repair enzymes can influence DNA repair capacity and, consequently, affect chemotherapy efficacy. We conducted this review to show the possible influence of the RAD51 genetic variants in damage repair capacity and treatment response in non-small-cell lung carcinoma patients.

Chemoradiotherapy

10.2217/pgs.13.48

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Citations (19)

Evaluation of 131 I-MIBG uptake in patients with neuroblastoma: Correlation with clinical follow-up

Augusto Nogueira Teresa Ferreira Lucas Resende Salgado M.R. Vieira

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